Type 2 diabetics are resistant to insulin in both muscle and liver. Both in vivo and in vitro studies indicate that chronic hyperglycemia is, in part, responsible for the defect in insulin action. In the present study, the investigators will examine whether chronically elevated plasma glucose levels are responsible for the excessive rate of basal hepatic glucose production in type 2 diabetics by acutely lowering the fasting glucose level with phlorizin, an inhibitor of renal glucose reabsorption. Total hepatic glucose production and glucose flux through glucose-6-phosphatase will be measured and gluconeogenesis will be monitored. This study is based on the hypothesis that, in poorly controlled type 2 diabetics, chronic hyperglycemia paradoxically may be the driving force for the accelerated rate of basal hepatic glucose production.